The biology of coronavirus COVID-19 - including research and treatments

[RedFox]

Independent Sage - COVID myths


https://www.independentsage.org/12-myths-about-covid-19-wheres-the-truth/

Myth #4 is "Long COVID is all in the mind":

As things stand currently – and this may change – there is no one specific blood test or X-ray that will say for sure that someone has Long COVID, and we don’t know why some people get it while others don’t. But this doesn’t mean the disease is imagined! It’s a real condition caused by underlying virus-induced changes. Various research studies have shown changes in the immune system, hormonal changes (particularly in cortisol levels), micro-clotting and changes that can be seen in, for example, MRI scans of the brain. These changes have been shown in some but not all people with Long COVID, suggesting that more than one pathway may be involved. Research is also ongoing to tease out the underlying pathways linking persistence of the virus to persistence of symptoms.

Watch Trish Greenhalgh’s response here.

 

[rvallee]

What I hate about the way this is framed is that it respects the traditional formula of: if we can't figure out the mechanism easily then it has to be psychological. It's the formula and everything behind it that's wrong. The idea that a scientific discipline could have a default explanation that is basically the modern equivalent of "God works in mysterious ways" is beyond absurd, it's basically anti-scientism.

There is no need for any of those abnormalities to be found to dismiss the nonsense about conversion disorder. It's a dumb 19th century myth devoid of any merit, it's not falsifiable, it has no scientific merit whatsoever. And this plays right into it, allowing for the never-ending process that has ruined everything before Long Covid came around, and continues to.

Hard to take anything from that Independent SAGE with Greenhalgh involved, frankly. She is probably a main reason they have been so bad at it from the start.

 

[SNT Gatchaman]

For a perhaps better overview of LC, I was pleased to watch UCSF's grand round "Unlocking the Mysteries of Long Covid" (YouTube, Oct 2022).

This was pleasing on a number of fronts, not least that UCSF has harboured some of the most egregiously minimising voices about the risks and realities of COVID and Long COVID. I liked the comment made that their research approaches are similar to the previously successful HIV model - although they hope for accelerated results rather than 20 years!

Dr Lekshmi Santhosh, UCSF (04:53) Syndrome description and demographics
Dr Michael Peluso, UCSF (15:38) Pathophysiological mechanisms - note zero reference to psychological factors in the presented hypotheses
Dr Ziyad Al-Aly, WUSTL (27:47) Overview of LC and their large scale VA epidemiological studies.

If interested but low on time capacity, I'd highlight the 2-5 minutes on hypothesised patho-mechanisms from 22:21.

 

[Mij]

Why are our government officials 'studying' whether we need to reinstate mask mandates with the increase of RVS, Covid and Flu overwhelming our ER's?

 

[Mij]

I'm seeing the term 'immunity debt' circulating on social media these last couple of weeks spreading misinformation.

Immunity debt hypothesis suggests that people's immune systems are weaker now due to lack of exposure to viruses from wearing masks, staying home and vaccines, so now our immunity is weaker to flu, RVS and Covid variants. This is dangerous misinformation.

 

[rvallee]

I'm seeing the term 'immunity debt' circulating on social media these last couple of weeks spreading misinformation.

Immunity debt hypothesis suggests that people's immune systems are weaker now due to lack of exposure to viruses from wearing masks, staying home and vaccines, so now our immunity is weaker to flu, RVS and Covid variants. This is dangerous misinformation.

Not just on social media. It's becoming official policy in some countries. Today I saw the French health minister blaming it for the current increase in respiratory illnesses. It's pretty much official in several other countries.

Basically pretending that people were living aseptic isolated lives for nearly 3 years. What nonsense. It's baffling that this doesn't get physicians screaming mad, and yet I see barely any pushback on it. Has there even been a study of how much, how long and how many people were truly at home for an extended period of time? It's been over for well over a year and other than disabled and immunocompromised almost no one was actually stuck at home in a real way, which no one cares about when it comes to us.

I've also seen this dude Prasad talk about how science and laboratory experiments aren't worth a damn, medicine needs to do RCTs of things like masks. It's hard to put in perspective exactly how much less reliable even solid RCTs are compared to real scientific experiments. There are trillions in economic activity that depend on understanding how air and gases work, how to filter particles and how to build and maintain clean rooms/plants. It's 100x more scientifically rigorous and tested in real life, and we have weirdos who think that RCTs, a significantly lesser and less reliable form of evidence, are better than actual rigorous science. What an incredible mess. Not surprisingly, same people who overhype a few anecdotes that validate their beliefs and ignore millions that don't.

It's clear that there are huge issues with scientific literacy in medicine. It's become a major problem. There would be little talk of pseudoscience like immunity debt, from the people who have pushed herd immunity no less, if not for professionals pushing for it. Same with all the pseudoscientific nonsense in the BPS ideology. This is really troubling and yet hardly anyone seems to even notice even as standards keep being degraded.

 

[Kitty]

Not just on social media. It's becoming official policy in some countries. Today I saw the French health minister blaming it for the current increase in respiratory illnesses.

What doesn't get said is that even if there were a bit of an uptick in people suffering from common respiratory viruses, for the most part it doesn't make much difference. These bugs circulate every year, large parts of the population can't realistically escape being exposed to at least some of them via family at home or colleagues at work, and most cause minor, self limiting illness. And for the small minority for whom all infections pose a serious risk, they'd still be a serious risk every winter with or without the intervention of a Covid pandemic. So what's the fuss about?

 

[Amw66]

 

[rvallee]

Clearly nothing a little CBT won't fix.

 

[Amw66]

My OH attended a doctor's on call / outpatient clinic ( it seemed to have morphed during daytime into a general clinic which GPs could refer to ) and was referred to dermatology for a rash ( assessed as a COVID booster side effect)

There were 4 other young women ( all under 40) at the initial clinic, all being treated for clots due to COVID.
He didn't know what the treatment was , ( he thought it was something that broke them up and let them go somewhere out of harm's way - he was a little preoccupied with himself to fully get the gist)

one woman had clots deemed " too big to break up " and had to attend weekly for 4-6 weeks for an alternative treatment.

Only women presenting - are clots more prevalent in female s?

 

[SNT Gatchaman]

[Preprint] SARS-CoV-2 protein NSP2 enhances microRNA-mediated translational repression (Belfast/Montreal team).

Viruses utilise miRNAs to impair the host antiviral immune system and facilitate viral infection by expressing their own miRNAs or co-opting cellular miRNAs.

non-structural protein 2 (NSP2) interacts with GIGYF2 [...] critical for blocking translation of the Ifn1-b mRNA that encodes the cytokine Interferon-ß, and thereby impairs the host antiviral immune response.

It is estimated that miRNAs target over 60% of human protein-coding mRNAs and affect important processes including development, cell proliferation, metabolism, and maintenance of homeostasis. Dysregulated miRNA expression and activity has been linked to diseases including cancer and metabolic disorders. Hence, control of miRNA-mediated translational repression by NSP2 during SARS-CoV-2 infection could have significant patho-physiological impacts.

 

[SNT Gatchaman]

[Preprint] Human iPS cell-derived sensory neurons can be infected by SARS-CoV-2 strain WA1/2020 as well as variants delta and omicron (MIT).

Peripheral neuropathies appeared as a specific COVID-19 symptom occurring at later stages of the disease. In order to understand the impact of SARS-CoV-2 on the peripheral nervous system, we generated human sensory neurons from induced pluripotent stem cells that we infected with the SARS-CoV-2 strain WA1/2020 and the variants delta and omicron. Using single cell RNA sequencing, we found that human sensory neurons can be infected by SARS-CoV-2 but are unable to produce new viruses.

 

[Sly Saint]

Scientists discover receptor that blocks COVID-19 infection

University of Sydney scientists have discovered a protein in the lung that blocks SARS-CoV-2 infection and forms a natural protective barrier in the human body.
This protein, the leucine-rich repeat-containing protein 15 (LRRC15), is an inbuilt receptor that binds the SARS-CoV-2 virus without passing on the infection.

The research opens up an entirely new area of immunology research around LRRC15 and offers a promising pathway to develop new drugs to prevent viral infection from coronaviruses like COVID-19 or deal with fibrosis in the lungs.

The study has been published in the journal PLOS Biology. It was led by Professor Greg Neely with his team members Dr. Lipin Loo, a postdoctoral researcher, and Ph.D. student Matthew Waller at the Charles Perkins Centre and the School of Life and Environmental Sciences.

The University study is one of three independent papers that reveal this specific protein's interaction with COVID-19.

"Alongside two other groups, one at Oxford, the other at Brown and Yale in the U.S., we found a new receptor in the LRRC15 protein that can stop SARS-CoV-2. We found that this new receptor acts by binding to the virus and sequestering it which reduces infection," Professor Neely said.

"For me, as an immunologist, the fact that there's this natural immune receptor that we didn't know about, that's lining our lungs and blocks and controls virus, that's crazy interesting."

"We can now use this new receptor to design broad acting drugs that can block viral infection or even suppress lung fibrosis."

What is LRRC15?
The COVID-19 virus infects humans by using a spike protein to attach to a specific receptor in our cells. It primarily uses a protein called the angiotensin-converting enzyme 2 (ACE2) receptor to enter human cells. Lung cells have high levels of ACE2 receptors, which is why the COVID-19 virus often causes severe problems in this organ of infected people.

Like ACE2, LRRC15 is a receptor for coronavirus, meaning the virus can bind to it. But unlike ACE2, LRRC15 does not support infection. It can, however, stick to the virus and immobilize it. In the process, it prevents other vulnerable cells from becoming infected.

"We think it acts a bit like Velcro, molecular Velcro, in that it sticks to the spike of the virus and then pulls it away from the target cell types," Dr. Loo said.

"Basically, the virus is coated in the other part of the Velcro, and while it's trying to get to the main receptor, it can get caught up in this mesh of LRRC15," Mr. Waller said.

https://phys.org/news/2023-02-scientists-receptor-blocks-covid-infection.amp

 

[Mij]

I'm seeing the term 'immunity debt' circulating on social media these last couple of weeks spreading misinformation.

These are the same people saying that masks aren't effective

I'm only wearing respirator N95 masks from now on. I got Covid or Influenza December 4th after going into store wearing a triple cloth mask for only 13 minutes.

I'm still dealing with this virus but it's slowly getting better.

 

[SNT Gatchaman]

SARS-CoV-2 infection of thymus induces loss of function that correlates with disease severity (2023, J Allergy Clin Immunology)

We showed that patients with COVID-19 had reduced thymic function that was inversely associated with the severity of the disease. We found that angiotensin-converting enzyme 2, through which SARS-CoV-2 enters the host cells, was expressed by thymic epithelium, and in particular by medullary TECs. We also demonstrated that SARS-CoV-2 can target TECs and downregulate critical genes and pathways associated with epithelial cell adhesion and survival.

 

[SNT Gatchaman]

Performance of RATs with Omicron variants —

Clinical performance of rapid antigen tests in comparison to RT-PCR for SARS-COV-2 diagnosis in Omicron variant: A systematic review and meta-analysis (2023, Reviews Medical Virology, pay-walled)

The pooled specificity and sensitivity of RATs were 1.000 (0.997–1.000) and 0.671 (0.595–0.721), respectively.

Add:

The sensitivity for samples with a CT-value >25 was 0.108 (0.048–0.227). Rapid antigen tests show impaired performance for COVID-19 diagnosis when the Omicron variant is circulating, particularly in samples with low viral loads.

 

[SNT Gatchaman]

Preprint: SARS-CoV-2 viral replication persists in the human lung for several weeks after onset of symptomatic severe COVID-19 and is associated with attenuated pulmonary immunity and variant-specific clinical sequalae

This, hitherto, undescribed bio-phenotype of lung-specific persisting viral replication was associated with an enhanced pulmonary pro-inflammatory response and variant-specific increased rates of bacterial bronchopneumonia and accelerated death. These findings question existing paradigms and suggest that in a subset of patients, concurrent, rather than sequential active viral replication continues to drive a heightened pro-inflammatory response.

 

[Sly Saint]

Rats can carry Covid, new study reveals

Rats can be infected with the Alpha, Delta and Omicron variants of Covid-19, a study has found.

Research published in the American Society for Microbiology found wild rats in New York city have been exposed to the virus.

The US Department of Agriculture and Animal and Plant Health Inspection Service tested samples from 79 Norway rats to look for evidence of Covid-19 infection.

They found that there was a possible link to the viruses that were spreading among humans during the early stages of the pandemic.

The rats were mostly trapped in city parks in Brooklyn, but some were captured near buildings.

Out of 79 rats, 13 tested positive for Covid-19.
The researchers found that Alpha, Delta and Omicron variants can cause infection in rats, including “high replication levels in the upper and lower respiratory tracts and induction of both innate and adaptive immune responses”.

Dr Henry Wan, a professor and director of the Center for Influenza and Emerging Infectious Diseases at the University of Missouri, said: “To the best of our knowledge, this is one of the first studies to show SARS-CoV-2 variants can cause infections in the wild rat populations in a major US urban area.”
He added: “Our findings highlight the need for further monitoring of SARS-CoV-2 in rat populations for potential secondary zoonotic transmission to humans.

“Overall, our work in this space shows that animals can play a role in pandemics that impact humans, and it’s important that we continue to increase our understanding so we can protect both human and animal health.”

Rats can carry Covid, new study reveals (msn.com)

 

[Sly Saint]

Covid origins: Chinese scientists publish long-awaited data

A research team in China has published analysis of samples taken more than three years ago from the market linked to the outbreak of Covid-19.

The Huanan seafood and wildlife market has been a focal point in the search for the origin of the coronavirus.

But this is the first peer-reviewed study of biological evidence gathered from the market back in 2020.

By linking the virus with animals sold in the market, it could open new lines of inquiry into how the outbreak began.

The research reveals swabs that tested positive for the virus also contained genetic material from wild animals.

Some scientists say this is further evidence that the disease was initially transmitted from an infected animal to a human.

But others have urged caution in interpreting the findings and it remains unclear why it took three years for the genetic content of the samples to be made public.

https://www.bbc.co.uk/news/science-environment-65204169

 

[CRG]

Covid origins: Chinese scientists publish long-awaited data

https://www.bbc.co.uk/news/science-environment-65204169

If the market wasn't the source of COVID 19, it nevertheless constituted a serious ongoing public health threat for the spread of known and novel zoonoses. (my bolding)

"The HSM is located in the Jianghan District in the downtown area of Wuhan, the capital city of Hubei Province, and is approximately 800 m away from Hankou Railway Station, a major railway travel hub. It occupies >50,000 m2 , with 678 stalls located close to each other in extremely crowded conditions (Fig. 1A). The market is separated into two zones, the East and West Zones, with seafood and animals mainly sold in the West Zone
and livestock meat in the East Zone. Among the 678 stalls of the market, 10 stalls selling domesticated wildlife (1.5%) were identified according to sale records 24, located in the south-western corner of West Zone (8/10) and the north-western corner of East Zone (2/10), respectively (Fig. 1A). According to sale records, during late December 2019, animals or animal products were sold in these 10 animal stalls. Animals included snakes,
avian species (chickens, ducks, gooses, pheasants and doves), Sika deer, badgers, rabbits, bamboo rats, porcupines, hedgehogs, salamanders, giant salamanders, bay crocodiles and Siamese crocodiles, etc., among which snakes, salamanders and crocodiles were traded as live animals (described in detail in the Report of WHOconvened global study of origins of SARS-CoV-2 24 ).

Out of the 923 environmental samples collected in and around the HSM, 73 were found by the real-time polymerase chain reactions (RT-PCR) to be positive for SARS-CoV-2 with positivity rate of 7.9%. Cycle threshold (CT) values for the RT-PCR ranged from 23.9 to 41.7 (Supplementary Table 2). Among the 828 samples inside the HSM, 64 samples (7.7%) were positive. Of the 64 SARS-CoV-2 positive samples collected inside the HSM, 87.5% (56/64) were collected in the West Zone of the market, in particular streets from no. 1 to 8, with 71.4% (40/56) positive samples identified herein (Fig. 1A). Among the 14 samples from warehouses related to the HSM, five tested positive. This may reflect the nature of SARS-CoV-2 presence in the market during the early phase of the outbreak. Among the 51 samples from sewerage wells (Supplementary Table 1) in the surrounding areas outside the HSM, three tested positive (Supplementary Table 2). Notably, one sample (Env_0601), a floor surface swab, out of the 30 environmental samples collected from Dongxihu Market in Wuhan on January 22nd 2020, also tested positive (Supplementary Table 2, Extended Data Table 4.

Of the 110 samples collected from sewers or sewerage wells in the market, 24 samples were positive for SARS-CoV-2 nucleic acid. All four sewerage wells in the market tested positive. During the onsite investigation of the overground drainage pathway in the HSM, we found that the wastewater in the overground drainage led into the underground drainage inside the market and then flowed into the wells on the edge of the market. We then did a spot-check sampling across all the overground drains according to the principles described in the Methods (Extended Data Fig. 1). Excreta of the upper respiratory tract of infected humans and the potential animal waste would be mixed together into the overground drainage. Thus, these data suggested that either infected people and/or animals in the market contaminated the sewage or that the contaminated sewage may have further played a role in furthering the virus transmission within the case cluster in the market."